Sebum normally constitutes a hydrating agent of the epidermis.
It is the natural product of the sebaceous gland, which is an appendage of the pilosebaceous unit. It is essentially a more or less complex mixture of lipids. Classically, the sebaceous gland produces squalene, triglycerides, aliphatic waxes, cholesterol waxes, and possibly free cholesterol (Stewart, M. E., Semin Dermatol 11, 100-105(1992)). The action of bacterial lipases converts a variable proportion of the triglycerides formed to free fatty acids.
The sebocyte constitutes the working cell of the sebaceous gland. The production of sebum is associated with a programme of terminal differentiation of this cell. During this differentiation, the metabolic activity of the sebocyte is essentially directed towards the biosynthesis of lipids (lipogenesis) and more precisely towards fatty acid neosynthesis.
Greasy hyperseborrhoeic skin is characterized by excessive secretion and excretion of sebum. Classically, an amount of sebum greater than 200 μg/cm2 measured on the forehead is regarded as characteristic of greasy skin. Such skin is in addition often associated with deficiency of desquamation, a glistening complexion, a thick skin texture, manifestations that are regarded as skin imperfections or aesthetic disorders.
Apart from its aspect of unsightliness, it is an area where complications may develop. It affects the zones where there is a high density of sebaceous glands and results principally from androgenic overstimulation of sebaceous production by these specific glands. Thus, hyperseborrhoea may also participate in the appearance of the lesions of acne vulgaris.
Acne vulgaris is a multifactorial disease that affects the areas of the skin with a high density of sebaceous glands (face, scapular region, arms and intertriginous regions). It is one of the commonest dermatoses.
In its mildest form, this dermatosis affects almost every human being. It is commonest at puberty, but it can be manifested for the first time starting from age 7 to 9 years and up to ages greater than 40 years. Moreover, it affects both men and women.
Among its commonest forms, we may mention acne simplex (acne vulgaris), generally called common acne, acne papulosa and/or nodular acne, acne conglobata and “exogenous” acne, appearing as a reaction to external inflammatory factors.
More precisely, acne is a disease of the follicle of the sebaceous gland. The following five pathogenic factors play a determining role in the constitution of acne:                genetic predisposition,        overproduction of sebum (seborrhoea),        androgenic,        disorders of follicular keratinization (comedogenesis), and        bacterial colonization and inflammatory factors.        
In fact, in the deepest parts of the infundibular portion of the hair follicle, we find there is formation of an above-normal quantity of keratinocytes. These cells differentiate into horn cells which progressively obstruct the lumen of the follicular canal. The physiological process of continuous desquamation from the acro-infundibulum to the surface is disturbed by the increased adherence of the horn cells produced. There is formation of a hyperkeratosic plug, constituting the comedo, the initial lesion of acne. Finally the three predominant local bacteria, Staphylococcus epidermidis, Malassezia furfur and Propionibacterium acnes find an ideal nutrient medium in the sebaceous follicle. The change in the environment and improvement of the conditions for growth of the microflora lead to an increase in pro-inflammatory products such as lipases, proteases, and interleukins. It is assumed that the lipases produced cause dissociation of the triglycerides to free fatty acids which, acting as irritants to the follicular epithelium, subsequently stimulate hyperproliferation. Promoting intensification of the inflammatory process, the granulocytes are attracted and migrate into the lumen of the follicle, where they finally contribute to the enzymatic disruption of the follicle wall.
The clinical manifestations of so-called retention that occur can be of the open or closed comedo type (microcyst, microcomedo, whitehead). The inflammatory lesions resulting from retention lesions can be papules, pustules, with indurated nodules, abscesses, fistulae, cicatricial states.
Thus, subjects with acne or who are susceptible to acne most often have greasy skin, skin that tends towards greasiness, or mixed. Their skin is most often glistening with numerous imperfections including those of the face (microcyst, microcomedo, whitehead, papules, pustules, with indurated nodules, abscesses, fistulae, and cicatricial states). The imperfections can also include skin that is sallow, with a muddy complexion, with dyschromia, redness, and rough skin with plaques of dry skin. There is cutaneous hyperkeratosis, on the face the pores are dilated, and the skin is often rough with a thick stratum corneum showing areas of dry skin in patches (epidermal atrophy and mild desquamation).
Accordingly, hyperseborrhoea is clearly a biological phenomenon that appears to require effective control to prevent the manifestation of associated skin disorders.
To combat hyperseborrhoea, various compounds have already been proposed which, by topical application on the skin, are able to reduce lipogenesis in the sebocytes and hence limit the production of sebum.
Unfortunately the treatments currently available are not completely satisfactory, notably with regard to side effects with which they are frequently associated such as irritation with certain topical products such as the retinoids and benzoylperoxides, or even gastrointestinal side effects (oral antibiotic therapy). Moreover, resistance of P. acnes to certain local antibacterial therapies is often observed.